Skin autoimmunity and blood coagulation

Evidence exists that the immune and coagulation systems are simultaneously activated in some systemic autoimmune disorders. Although proinflammatory mediators induce tissue factor (TF) expression, the main initiator of blood coagulation, activated proteases of coagulation may act on protease-activated receptors (PAR) triggering inflammation. Such a cross-talk amplifies and maintains the activation of both systems. This review focuses on the involvement of immune and coagulation system in two skin disorders as chronic urticaria (CU), autoimmune in about 45% of cases, and bullous pemphigoid (BP), the prototype of autoimmune blistering diseases. Several investigators demonstrated the activation of coagulation in CU through the involvement of eosinophils, of TF pathway with thrombin generation and increased vascular permeability. Preliminary data indicate that anticoagulant treatment with heparin and warfarin may be effective in reducing the symptoms of this disorder. The activation of coagulation seems to display local and systemic implications in BP. Eosinophils' recruitment and thrombin generation locally contribute to the bulla formation and tissue damage. The systemic activation of coagulation may explain the increased thrombotic risk observed in these patients. Taken together, these data provide the rationale for proposing clinical trials on the anticoagulant treatment in both CU and BP patients.     

钙卫蛋白在炎性疾病中的表达及临床意义

炎性疾病作为临床常见病种,关于其诊断和治疗已成为医学研究中的一项重要任务.钙卫蛋白是一种由中性粒细胞所分泌,与炎症反应紧密相关的钙锌结合蛋白.随着近年来医学的发展,钙卫蛋白作为一种新的检测手段越来越受到重视.国内外已有较多有关钙卫蛋白与炎症性肠病、肝病、自身免疫病等炎性疾病关系的报道.研究表明,钙卫蛋白与上述疾病的严重程度明显相关,并可用来预测此类疾病的预后及复发情况.     

The significance of T suppressor cells in the development of autoimmunity

Despite intensive research, autoimmune-disease pathogenesis is still an enigma, but in the past decade Ts-cell defects have assumed a central role in this pathogenesis. Ts-cell dysfunctions have been reported in numerous autoimmune diseases (e.g. SLE, autoimmune thyroid disease, myasthenia gravis) and in animal models of autoimmune diseases. Therefore, it is currently believed that Ts cells are responsible for maintaining self-tolerance and that perturbations in suppressor functions may initiate development of autoimmune diseases. Ts-cell abnormalities can result from LCTA production, intrinsic biochemical alterations, genetic susceptibility, or environmental factors. Since Ts-cells dysfunctions are believed to initiate autoimmunity, it may be possible to treat autoimmune diseases by correcting the suppressor defects, and indeed, preliminary trials in this direction are promising.     

The anti-Sm immune response in autoimmunity and cell biology

Anti-Sm antibodies are found in greater than 30% of the patients with systemic lupus erythematosus (SLE) and are diagnostic of SLE. The Sm autoantigens are the small nuclear ribonucleoprotein (snRNP) common core proteins. The seven core proteins, B, D1, D2, D3, E, F and G, shared by a majority of the snRNP particles, form a heptamer ring approximately 20 nm in diameter, with the snRNA passing through the center. The Sm epitopes are distributed on the outside surface of the ring. A repeated proline rich motif with homology to an Epstein bar nuclear antigen in the B protein and a gly-arg-gly motif including a symmetrical dimethylarginine post translational modification in the B, D1 and D3 proteins are major Sm epitopes. The anti-Sm response has features typical of an antigen driven immune response. SnRNP proteins share several characteristics with other autoantigens including their assembly into ribonucleoprotein particles, homologies to known viral proteins, presence of post translational modifications, a high abundance and great stability and the presence of repeated motifs. Current work on the snRNP particles is attempting to identify the features that predispose the common core proteins to become autoantigens in vulnerable individuals.     

The relationship between coagulation state and inflammatory bowel disease: current understanding and clinical implications

Inflammatory bowel disease (IBD) is associated with a hypercoagulable state and subsequently with an increased risk for venous thromboembolism (VTE). VTE in IBD is characterized by a high recurrence rate and is associated with the disease activity. Acquired endothelial dysfunction, abnormalities of platelets, activation of coagulation system and impaired fibrinolysis are the main changes in the coagulation state in IBD. The development of VTE in IBD has been considered to be the result of multiple interactions between acquired and inherited risk factors. The treatment of VTE in IBD patients is recommended to be similar and to follow the same protocols as for non-IBD patients. In the clinical practice, the management of IBD patients and especially the hospitalized patients should include thromboprophylaxis.     

The airway inflammatory response in allergic asthma and its relationship to clinical disease

Endobronchial biopsy and lavage studies have revealed the presence of mast cell, eosinophil, T-lymphocyte and epithelial cell activation in asthma, along with the structural changes of tissue eosinophil infiltration, loss of superficial columnar ciliated epithelial cells and enhanced collagen deposition in the laminar reticularis. As these cellular and structural changes underlie the clinical features of asthma, i.e., symptom expression, variable airflow obstruction and bronchial hyperresponsiveness, an understanding of their induction and regulation is essential to the understanding of the asthmatic process. The acute airway response to allergen has been studied by the technique of local endobronchial allergen challenge with direct airway sampling in asthma. These studies identify allergen-mast cell interaction as the initial airway event, with mediator release inducing bronchoconstriction and enhancing vascular permeability. As preformed cytokines are present in mast cells, cytokine release from this cell population is likely to initiate the process of endothelial cell activation, with upregulation of cell adhesion molecules, and tissue cell recruitment. Subsequent cytokine elaboration from airway macrophages and T-lymphocytes will perpetuate this response while in chronic clinical disease T-lymphocytes, mast cells, matrix tissue, epithelial cells and eosinophils themselves are all likely to contribute to the cytokine pool within the airways and thus to the regulation of inflammatory cell migration and activation.     

颈椎内固定后早期炎症指标的变化趋势及临床意义

背景：脊柱内固定后感染是其严重并发症,多项研究表明血沉及C-反应蛋白在判断感染方面具有重要意义。目的：文章分析颈椎内固定后无感染患者血沉及C-反应蛋白的变化趋势。方法：回顾性分析2013年10月至2014年7月收治的颈椎内固定患者56例,根据内固定方式分为2组,颈椎前路组为行颈椎前路减压植骨融合内固定的患者29例,颈椎后路组为行颈椎后路单开门减压内固定患者27例。内固定前、内固定后第1,3,6,9天清晨采集患者外周血,检测血沉及C-反应蛋白值,随访超过1年,未出现感染迹象。结果与结论：①一般规律：颈椎内固定后,患者血沉在第6天显著升高并达到峰值,随后逐渐下降,第9天仍未降至正常;C-反应蛋白在第3天显著升高并达到峰值,随后迅速下降,第9天仍未降至正常;颈椎后路组患者内固定后第3,6,9天血沉水平明显高于颈椎前路组(P < 0.05),C-反应蛋白差异无显著性意义(P > 0.05)。②结果说明,C-反应蛋白是颈椎内固定后监测患者炎症反应的重要指标,有助于内固定后早期感染的判断。内固定后早期血沉及C-反应蛋白2种炎症指标的异常,并不提示内固定后刀口感染的存在。C-反应蛋白可在内固定后第3天达到峰值,建议在第2,3天查血,随后如无明显反弹,则感染可能性小;内固定后炎症指标下降后再次升高或下降缓慢,可能提示感染的存在。  中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程     

Innate lymphoid cells in autoimmunity and chronic inflammatory diseases

Seminars in Immunopathology - Abnormal activation of the innate immune system is a common feature of autoimmune and chronic inflammatory diseases. Since their identification as a separate family of...     

凝血因子Ⅴ在重型肝炎患者中的检测及其临床意义

目的　了解凝血因子Ⅴ (Ⅴ因子 )在重型肝炎预后因素中的作用及其在临床诊断标准中的意义。方法　通过比浊法对 5 8例重型肝炎患者进行了 12 9例次Ⅴ因子活性检测 ,并与同期凝血酶原活动度 (PTA)水平进行对比研究 ;以SPSS及SDAS软件对检测结果进行分析。结果　发生重型肝炎时Ⅴ因子和PTA水平分别为 15 3%± 9 7%及 2 3 5 %± 10 0 % ,随着病情的加重Ⅴ因子或PTA水平逐渐降低 ,病死率均逐渐升高 ,差异有非常显著意义 (P =0 0 0 0 ) ;死亡者Ⅴ因子及PTA水平逐步迅速降低 ,而存活者则逐渐升高。在病情加重或恢复时 ,PTA较Ⅴ因子先下降或先上升 ;在 14例 (2 4 14 % )出现肝性脑病的患者中 ,10例 (92 86 % )在病程终末期出现 ,远晚于Ⅴ因子水平下降的时间 ;通过分析可知 ,Ⅴ因子水平与PTA水平高度相关 (相关系数 0 812 ) ,临床测定值基本一致。结论　Ⅴ因子水平可作为重型肝炎预后的一个重要预后因素 ,较PTA水平更为特异。因此 ,同时测定PTA及Ⅴ因子水平 ,可以更早地、更准确地诊断重型肝炎 ;同时应加强重型肝炎患者Ⅴ因子的检测及重视Ⅴ因子在作为肝衰竭患者行肝移植术时的主要筛选指标的研究     

胎盘炎性病变的分类、病理特征及临床意义

胎盘功能之一是保护胎儿免受感染.母体和胎儿炎性反应引起的胎盘炎性改变应被准确记录和诊断,这是胎盘最常见的病理改变,包括由感染因素引发的感染性炎性病变以及无明确感染病因的特发性/免疫性炎性病变.胎盘炎性病变分为绒毛膜羊膜炎、绒毛炎、绒毛间隙炎等.本篇综述将从分类、病理特征及临床意义三个方面进行系统的描述.     

New insights into the biological and clinical significance of fecal calprotectin in inflammatory bowel disease

Nowadays, calprotectin, a cytoplasmatic protein, released by activated neutrophilic polymorphonuclear cells (PMN) and/or monocytes-macrophages (M?), is considered a good indicator of inflammation in several diseases. Accordingly, fecal calprotectin represents a good predictor of clinical relapse in ulcerative colitis (UC) patients, whereas conflicting results have been reported in Crohn's disease (CD) patients. In our study, in 76 IBD patients (29 CD and 47 UC) fecal calprotectin has been evaluated by a commercial ELISA kit. Results demonstrate that levels of this protein in the stool are significantly more elevated in active CD and UC patients than in normal volunteers. In quiescent CD and UC a trend to higher levels of calprotectin than in the normal counterpart is, however, evident. These data suggest that a low-grade inflammation of the intestinal wall is always present in CD and UC patients, which may predict a clinical relapse risk. In the same group of patients calprotectin levels also were analyzed according to sex and age. A trend to higher values of calprotectin was present in male patients with active or quiescent CD than in their female counterparts. Only in UC patients in remission a trend to calprotectin increase was more marked in the male group than in the female counterpart. When CD and UC patients were divided up according to age, calprotectin positivity peaked between 30-39 years in active CD patients, while in quiescent CD maximum positivity was between 40 and 49 years. However, in both active and quiescent UC patients, calprotectin positivity increased with age. The more precocious detectability of fecal calprotectin in CD patients, as a marker of intestinal mucosa inflammation, may be related to the different histopathology of the two diseases (CD versus UC). However, reduced PMN and/or M? trafficking from peripheral blood to intestinal mucosa with age by effects of chronic treatment should not be ignored in CD patients.     

炎症反应在冠心病患者中的作用及临床意义

目的 :探讨炎症反应与冠心病 (CHD)之间的关系。方法 :10 1例CHD患者分为 3组 ,即稳定型心绞痛 (SAP)组 (19例 )、不稳定型心绞痛 (UAP)组 (33例 )和急性心肌梗死 (AMI)组 (49例 )。分别采用免疫浊度法及血细胞计数仪 ,检测外周血中的C 反应性蛋白 (CRP)水平及白细胞 (WBC)总数。 2 0例AMI死亡患者的心肌组织切片进行病理学检查。结果 :AMI和UAP组血中CRP的水平和WBC总数明显高于对照组 (P <0 .0 1)。病理学检查发现 ,AMI患者心肌中有大量白细胞浸润。结论 :CHD发生、发展有炎症反应的参与 ,检测血中的CRP和WBC可作为监测病情、预测冠心病危险性的常规指标之一     

Poly-2-methoxyethylacrylate-coated bypass circuits reduce activation of coagulation system and inflammatory response in congenital cardiac surgery

Surface-coated cardiopulmonary bypass (CPB) has been shown to have excellent biocompatibility during cardiac surgery in adults, but there have been only a few reports demonstrating the efficacy of this coating for congenital cardiac surgery. We tested the efficacy of poly-2-methoxyethylacrylate (PMEA) coating for CPB circuits in congenital cardiac surgery. Eleven operative cases of ventricular septal defect were studied: group C (control: no coating, n = 5) and group P (PMEA coating, n = 6). The platelet count and beta-thromboglobulin (beta TG), fibrinogen (FBG), thrombin-antithrombin complex (TAT), and neutrophil elastase levels were measured during the operation. Postoperative chest tube drainage was analyzed and the surface of the artificial lung was observed with an electron microscope. Elevation of TAT and neutrophil elastase was suppressed in group P (P < 0.05). Observation of the artificial lung surface using an electron microscope clearly revealed fewer blood cells were adherent to the surface in group P. The FBG level and postoperative bleeding were relatively lower in group P, but there were no significant differences between groups. The platelet count and beta TG level were the same in both groups. We concluded that the PMEA-coated circuit reduces activation of the coagulation system and the inflammatory reaction in pediatric cardiac surgery.